Here is some R code simulating this with random data where NII-RF is correlated to age and to ME/CFS status:
Output:
To get an idea of what the p-values are, I looked at the ANOVA results for the last trial:
When comparing the models without age, the p-value was 0.48. With age, it was 0.03.
In the case of models 3 and 4, we can be more confident about the amount that ME/CFS status improves the model, since the age variable is included and can explain some of the variance.
I'm not able to right now, but I might code it with simulated data later. It should be relatively...
I'm not sure what exactly you mean by the p-value of the initial model. The p-value of the ME/CFS status coefficient in a model including all covariates? I think this is the same p-value you would get from an F-test comparing the model with and without ME/CFS status.
Yes, but this is in the case of age being correlated to both ME/CFS status and NII-RF. Age can be correlated to only NII-RF, in which case adding this variable to a model that only had ME/CFS does lead to better predictive ability for NII-RF.
Yeah, decreased standard error for the coefficient of the main exposure on the outcome since some of the noise is accounted for by the covariate.
Edit: This goes a bit into it, talking about how controlling for covariates increases precision...
I also wasn't sure why it would be necessary to match group size.
Are they saying they excluded ME/CFS participants that didn't have similar metrics to a healthy control? Or they just randomly removed ME/CFS participants to match group size?
Either way, I don't really see the reason for doing...
I don't think it's an issue. Often significance decreases after controlling for a variable because a covariate is correlated to both the exposure and the outcome, so it explains part of the relationship. But significance can increase if controlling for a covariate that is mainly correlated to...
A gain-of-function Retsat variant from high-altitude adaptation promotes myelination via a neuronal dihydroretinoic acid-RXR-γ pathway, 2026, Li et al
A gain-of-function Retsat variant from high-altitude adaptation promotes myelination via a neuronal dihydroretinoic acid-RXR-γ pathway...
Here is the VRK2 variant they highlighted in the text, rs7596038 (2-58156685-C-T), highlighted over the DecodeME data:
It doesn't look to be within the main ME/CFS locus.
Though it's interesting that there are two loci with somewhat significant lead variants in ME/CFS around this area. Maybe...
Cross-ancestry genetic architecture reveals shared biological pathways of major psychiatric disorders
Abstract
Psychiatric disorders, including bipolar disorder (BD), major depressive disorder (MDD), and schizophrenia (SCZ), share substantial genetic overlap. We conducted a cross-ancestry...
Similarly titled paper from a few years ago: Molecular Hydrogen as a Medical Gas for the Treatment of Myalgic Encephalomyelitis/CFS: Possible Efficacy Based on a Literature Review, 2022, Hirano
None of the details of the exercise trials are in the paper, so I wanted to check the supplementary material, but I can't find Appendix 1. I see a file called "Supplementary file 1.docx" which includes "Appendix A: Search terms for the living database", but it doesn't seem to have Appendix 1.
I'm just starting with reading the abstract, but this directionality is reversed for between-group vs within-ME/CFS, right? If so, I think this would make the finding less compelling.
I like that they are continuing to do the open-label study at the same time, for more immediate, even if less reliable, results. A steady drip of unblinded results until finally revealing the blinded results.
Intersectionality, healthcare and myalgic encephalomyelitis: Reflections from experience
Hunt, Joanne
Abstract
Healthcare practice and policy impacting disabled groups has historically reduced disability to an individual phenomenon and homogenised experiences of disability.
Such practices –...
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